Publications by authors named "Maria Luisa Muci"

10 Publications

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Oxygen extraction ratio to identify patients at increased risk of intradialytic hypotension.

Sci Rep 2021 Feb 26;11(1):4801. Epub 2021 Feb 26.

Department of Translational and Precision Medicine, Nephrology Unit at Policlinico Umberto I Hospital, "Sapienza" University of Rome, Viale del Policlinico 155, 00161, Rome, Italy.

Intradialytic hypotension (IDH) is a hemodynamic phenomenon recently associated with decreased blood oxygen saturation (SO). The ratio between peripheral oxygen saturation (SpO) and central venous SO (ScvO) or Oxygen Extraction Ratio (OER), which represents a roughly estimate of the amount of oxygen claimed by peripheral tissues, might be used to estimate haemodialysis (HD) related hypoxic stress. Aim of this pilot study was to evaluate the relationship between OER increments during dialysis sessions (ΔOER) and episodes of IDH. We enrolled chronic HD patients with permanent central venous catheter (CVC) and no fistula, in whom ScvO measurement is at hand. OER ([(SpO - ScvO)/SpO] × 100) was measured in three consecutive HD sessions (HD OER sessions) before HD, after 15', 30' and 60' min and at the end of HD. Then, a one-year follow-up was planned to record the number of IDH episodes. In the 28 enrolled patients (age 74 ± 2.6 years), during 12 ± 1.2 months of follow up, incidence of IDH was 3.6%. We divided patients into two groups, above or below the median value of ΔOER at the end of HD, which was 36%. In these groups, the average incidence of IDH was 7% and 2% respectively (p < 0.01), while OER values before HD were not different. Notably, in the high ΔOER group the OER increment was evident since after 15' and was significantly higher than in the low ∆OER group (∆OER-15' = 19 ± 3.0% vs. 9.0 ± 3.0%; p < 0.05). By comparison, blood volume changes overlapped in the two groups (average change - 9 ± 0.8%). Values of ∆OER > 19% after only 15' of HD treatment or > 36% at the end of the session characterize patients with higher rates of hypotension. Intradialytic ∆OER, a parameter of tissue hypoxic stress, identifies more fragile patients at greater risk of IDH.
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http://dx.doi.org/10.1038/s41598-021-84375-7DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7910620PMC
February 2021

A new technique for measuring fistula flow using venous blood gas oxygen saturation in patients with a central venous catheter.

Clin Kidney J 2020 Apr 1;13(2):184-187. Epub 2019 Jun 1.

Nephrology and Dialysis Unit, ICOT Hospital, Polo Pontino Sapienza University of Rome, Italy.

Background: Doppler ultrasound (DU) monitoring early after arteriovenous fistula (AVF) creation allows the identification of low blood flow (Qa) requiring prompt revision, but it is costly (needs skilled operators and technical instruments) and is not available in all dialysis units. Therefore alternative first-line methods to measure Qa would be welcomed. We reasoned that once an AVF is created, an increment in central venous oxygen saturation (ScvO) is predictable and proportional to Qa.

Methods: Accordingly, in patients receiving dialysis through a central venous catheter (CVC) in whom an AVF was created, we measured, by means of blood gas analysis, the ScvO increment before and after manual compression of the arteriovenous shunt and verified its correlation with DU-measured Qa.

Results: We sampled blood gas in 18 patients with CVC and AVF before and after 30 s manual compression of the AVF. ScvO averaged 70.5 ± 3% before and 65.2 ± 3% after AVF closure, with an average drop of 5.1 ± 3% (range 1-12). AVF Qa, which was measured within 24 h by means of DU, averaged 635 ± 349 mL/min (range 50-1300) and was strictly and positively correlated with ΔScvO ( 0.954, P < 0.0001).

Conclusions: Therefore we suggest that in patients with CVC and a newly created AVF, it is possible to monitor AVF Qa without DU by simply measuring blood gas and ΔScvO. This technique is simple, cheap, repeatable, non-invasive and operator independent and represents a new useful screening test to detect delayed AVF access maturation deserving prompt DU measurement and surgical revision. It helps to quickly identify patients in urgent need of DU verification and possible surgical revision. Regrettably, it is applicable only in patients with CVC.
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http://dx.doi.org/10.1093/ckj/sfz064DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7147307PMC
April 2020

On the role of skin biopsy in the diagnosis of calcific uremic arteriolopathy: a case-based discussion.

J Nephrol 2020 Aug 2;33(4):859-865. Epub 2019 Dec 2.

Dialysis Unit at ICOT Hospital, Latina, Italy.

Calciphylaxis is a rare disease characterized by ectopic calcification of skin arterioles resulting in ischemia, thrombosis and necrosis. Since end stage renal disease patients are those mainly affected, the term calcific uremic arteriolopathy (CUA) is also suggested. Early clinical manifestations are subtle, while overt necrotic ulcers may quickly spread and become infected so as to result in ominous outcome. Diagnosis might not be easy due to the number of other ischemic and non-ischemic skin lesions observed in uraemia. Skin biopsy, has been proposed as the diagnostic test and is often considered, but not systematically performed due to the hypothetical risk of further spreading of the lesions. Such ambiguity could be responsible for misdiagnosis or underdiagnosis. We review here five consecutive cases recorded in our Unit, all submitted to skin biopsy but with inconsistent results which generated some clinical frustration. Thus, we decided to carefully re-evaluate all of them together with pathologists and dermatologists. However, even after this ex-post discussion, we could not reach a complete agreement on the final diagnosis. In the meanwhile, papers were published in the literature that started to shed some light on the role of skin biopsy in the diagnosis of CUA.
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http://dx.doi.org/10.1007/s40620-019-00678-zDOI Listing
August 2020

Oxygen Extraction Ratio (OER) as a Measurement of Hemodialysis (HD) Induced Tissue Hypoxia: A Pilot Study.

Sci Rep 2018 04 4;8(1):5655. Epub 2018 Apr 4.

Nephrology and Dialysis Unit, ICOT Hospital, Polo Pontino Sapienza University of Rome, Rome, Italy.

HD tissue hypoxia associates with organ dysfunctions. OER, the ratio between SaO and central-venous-oxygen-saturation, could estimate oxygen requirements during sessions, but no data are available. We evaluated OER behavior in 20 HD patients with permanent central venous catheter (CVC) as vascular access. Pre-HD OER (33.6 ± 1.4%; M ± SE) was higher than normal (range 20-30%). HD sessions increased OER to 39.2 ± 1.5% (M ± SE; p < 0.05) by 30' and to 47.4 ± 1.5% (M ± SE; p < 0.001) by end of treatment (delta 40%). During HD sessions of the long and short interdialytic intervals, OER values overlapped, suggesting no influence of patient's hydration status shifts. OER increased (p < 0.05) after 30' of isolated HD (zero ultrafiltration), but not during isolated ultrafiltration (zero dialysate flow), suggesting a role for blood-membrane-dialysate interaction, independent of volume reduction. In ten patients, individual variability of pre-HD OER was low and repeatable (maximum calculated difference over time 6.6%), and negatively correlated with HD-induced OER increments (r = 0.860; p < 0.005), suggesting a decline in the adaptive response along with resting OER increments. In 30 prevalent patients, adjusted multivariate analysis showed that pre-HD OER (HR = 0.88, CI 0.79-0.99, p = 0.028) and percent HD-induced OER (HR = 1.04, CI 1.01-1.08, p = 0.015) were both associated with mortality, with threshold values respectively <32% and >40%. In HD patients with CVC as vascular access, OER is a cheap, easily measurable and repeatable parameter useful to assess intradialytic hypoxia, and a potential biomarker of HD related stress and morbidity, helpful to recognize patients at increased risk of mortality.
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http://dx.doi.org/10.1038/s41598-018-24024-8DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5884820PMC
April 2018

Interactions of sclerostin with FGF23, soluble klotho and vitamin D in renal transplantation.

PLoS One 2017 30;12(5):e0178637. Epub 2017 May 30.

Department of Cardiovascular, Respiratory, Nephrologic, Anesthesiologic and Geriatric Sciences, Sapienza University of Rome, Italy.

Relationships of Sclerostin, a bone anti-anabolic protein, with biomarkers of mineral bone disorders in chronic kidney disease are still unsettled, in particular in kidney transplant (KTR). In 80 KTR patients (31F/49M, 54.7±10.3 years) we studied the relationships of serum Sclerostin with eGFR, Calcium, Phosphate, Alkaline Phosphatase (AP), intact Parathyroid hormone (iPTH), soluble alpha-Klotho (sKlotho), intact Fibroblast Growth Factor 23 (iFGF23), 25-hydroxyvitamin D(25D) and 1,25-dihydroxyvitamin D (1,25D). Thirty healthy subjects (35.0±12.4 years, eGFR 109.1±14.1 ml /min/1,73m2) served as control for Sclerostin, iFGF23 and sKlotho. With a median eGFR of 46.3 mL/min/1.73m2 (IQR, 36.2-58.3) our KTR had median Sclerostin levels of 23.7 pmol/L (IQR: 20.8-32.8), not different from controls (26.6 pmol/L, IQR: 22.0-32.2; p = n.s). Sclerostin correlated negatively with AP (r = -.251; p = 0.023) and positively with iFGF23 (r = .227; p = 0.017) and 25D (r = .214; p = 0.025). Age-adjusted multiple regression analysis identified AP and 1,25D as negative and 25D and sKlotho as positive best predictors of Sclerostin. No correlation was evident with eGFR. The negative correlation with AP confirms the direct anti-anabolic role of Sclerostin. The associations either negative or positive with iFGF23, sKlotho, and vitamin D metabolites suggest also a modulatory role in mineral homeostasis. In particular, the associations with iFGF23 (positive) and 1,25D (negative) underline the relevant inhibitory action of Sclerostin on vitamin D activation. In conclusion, Sclerostin levels in KTR are normal and influenced more by bone turnover than by eGFR. Its involvement with other hormones of mineral homeostasis (FGF23/Klotho and Vitamin D) is part of the sophisticated cross-talk between bone and the kidney.
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http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0178637PLOS
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5448809PMC
October 2017

Positioning novel biologicals in CKD-mineral and bone disorders.

J Nephrol 2017 Oct 24;30(5):689-699. Epub 2017 May 24.

Department of Cardiovascular, Respiratory, Nephrologic, Anesthetic and Geriatric Sciences, Sapienza University of Rome, Rome, Italy.

Renal osteodystrophy (ROD), the histologic bone lesions of chronic kidney disease (CKD), is now included in a wider syndrome with laboratory abnormalities of mineral metabolism and extra-skeletal calcifications or CKD-mineral and bone disorders (CKD-MBD), to highlight the increased burden of mortality. Aging people, frequently identified as early CKD, could suffer from either the classical age-related osteoporosis (OP) or ROD. Distinguishing between these two bone diseases may not be easy without bone biopsy. In any case, besides classical therapies for ROD, nephrologists are now challenged by the possibility of using new drugs developed for OP. Importantly, while therapies for ROD mostly aim at controlling parathyroid secretion with bone effects regarded as indirect, new drugs for OP directly modulate bone cells activity. Thus, their action could be useful in specific types of ROD. Parathyroid hormone therapy, which is anabolic in OP, could be useful in renal patients with low turnover bone disease. Denosumab, the monoclonal antibody against receptor activator of NF-κB ligand (RANK-L) that inhibits osteoclast activity and proliferation, could be beneficial in cases with high turnover bone. Use of romosozumab, the monoclonal antibody against sclerostin, which both stimulates osteoblasts and inhibits osteoclasts, could allow both anabolic and anti-resorptive effects. However, we should not forget the systemic role now attributed to CKD-MBD. In fact, therapies targeting bone cells activity could also result in unpredicted extra-bone effects and affect cardiovascular outcomes. In conclusion, the new biologicals established for OP could be useful in renal patients with either OP or ROD. In addition, their potential non-bone effects warrant investigation.
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http://dx.doi.org/10.1007/s40620-017-0410-1DOI Listing
October 2017

Calcitriol/calcifediol ratio: An indicator of vitamin D hydroxylation efficiency?

BBA Clin 2015 Jun 14;3:251-6. Epub 2015 Mar 14.

Department of Cardiovascular, Respiratory, Nephrologic, Anesthesiologic and Geriatric Sciences, Sapienza University of Rome, Italy.

Background: Calcifediol (25D) availability is crucial for calcitriol (1,25D) synthesis, but regulation of vitamin D hydroxylases is majorly responsible for 1,25D synthesis. The net efficiency of vitamin D hydroxylases might be informative. We assume that the ratio between calcitriol and calcifediol (25D/1,25D) serum concentrations could suggest the vitamin D hydroxylation efficiency.

Methods: We evaluated 25D/1,25D in different patient populations: hemodialysis (HD, n = 76), CKD stage 2-5 (n = 111), renal transplant (TX, n = 135), patients with no renal disease (No-CKD, n = 290), and primary hyperparathyroidism (PHP, n = 20).

Results: The geometric mean of 1,25D/25D (pg/ng) averaged 1.11 (HD), 1.36 (CKD), 1.77 (TX), 2.22 (No-CKD), and 4.11 (PHP), with a progressive increment from HD to PHP (p-value for the trend <0.001). Each clinical condition elicited a significant effect on 25D/1,25D (p < 0.0001) and adjusted multivariate analysis indicated levels of Cas, Ps, PTH, and 25D as predictors of 25D/1,25D. Both in vitamin D deficient and replete subjects (25D< or ≥20 ng/ml) 25D/1,25D associated with each clinical condition (p < 0.0001) and mean values increased progressively from HD to PHP (p-values for the trend <0.0001). Regression analysis between 25D (substrate) and 25D/1,25D (efficiency) revealed an exponential negative correlation in No-CKD (r(2)Exp = 0.53, p < 0.001) with sharp increments of 25D/1,25D when 25D values are <20 ng/ml. At variance, in CKD (r(2)lin = 0.19) and in TX (r(2)lin = 0.32) the regression was linear as if, in case of deficit, some inhibition of the system were operating.

Conclusion And General Significance: In conclusion 1,25D/25D can reflect the efficiency of vitamin D hydroxylases more than separate evaluation of 25D and 1,25D and can facilitate the therapeutic choices in different patient populations.
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http://dx.doi.org/10.1016/j.bbacli.2015.03.004DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4661572PMC
June 2015

Soluble α -Klotho Serum Levels in Chronic Kidney Disease.

Int J Endocrinol 2015 19;2015:872193. Epub 2015 Mar 19.

Department of Cardiovascular, Respiratory, Nephrology, Geriatric, and Anesthetic Sciences, "Sapienza" University, 5 Piazzale Aldo Moro, 00185 Rome, Italy.

Transmembrane α-Klotho (TM-Klotho), expressed in renal tubules, is a cofactor for FGF23-receptor. Circulating soluble-α-Klotho (s-Klotho) results from TM-Klotho shedding and acts on Phosphate (P) and Calcium (Ca) tubular transport. Decreased TM-Klotho, described in experimental chronic kidney disease (CKD), prevents actions of FGF23 and lessens circulating s-Klotho. Thus, levels of s-Klotho could represent a marker of CKD-MBD. To evaluate the clinical significance of s-Klotho in CKD we assayed serum s-Klotho and serum FGF23 in 68 patients (age 58 ± 15; eGFR 45 ± 21 mL/min). s-Klotho was lower than normal (519 ± 183 versus 845 ± 330 pg/mL, P < .0001) in renal patients and its reduction was detectable since CKD stage 2 (P < .01). s-Klotho correlated positively with eGFR and serum calcium (Cas) and negatively with serum phosphate (Ps), PTH and FGF23. FGF23 was higher than normal (73 ± 51 versus 36 ± 11, P < .0002) with significantly increased levels since CKD stage 2 (P < .001). Our data indicate a negative effect of renal disease on circulating s-Klotho starting very early in CKD. Assuming that s-Klotho mirrors TM-Klotho synthesis, low circulating s-Klotho seems to reflect the ensuing of tubular resistance to FGF23, which, accordingly, is increased. We endorse s-Klotho as an early marker of CKD-MBD.
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http://dx.doi.org/10.1155/2015/872193DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4383388PMC
April 2015

[Update on the pathogenesis and possible therapeutic approach to vascular calcifications in patients with chronic renal failure].

G Ital Nefrol 2011 Sep-Oct;28(5):514-24

Dipartimento di Scienze Cardiovascolari, Respiratorie, Nefrologiche e Geriatriche dell'Universita' Sapienza di Roma, Roma, Italy.

Chronic renal failure is a well-known risk condition for cardiovascular disease and in particular vascular calcifications. In fact, with respect to the normal population, where only ''classic'' risk factors have been described, kidney patients also have non-classic risk conditions. Among these, alterations in divalent ions, parathyroid hormone and vitamin D are of utmost importance. Further, several substances are recognized to have inhibitory or inductive effects in the pathogenesis of vascular calcifications, affecting either the calcium salts precipitation phenomenon or the phenotypic transformation of vascular smooth muscle cells into osteoblast-like cells (the latter phenomenon being regarded as a determinant of calcification of the tunica media). Given that vascular calcifications are irreversible, therapeutic strategies are aimed at preventing their formation or at blunting their progression (which is especially accelerated in renal patients). For this purpose it is essential to pursue optimal biochemical control of secondary hyperparathyroidism, but we must consider that in the individual patient the choice of drugs and their dosage can be essential for the development of calcifications. Given the physiological importance of inhibitory substances, we can hypothesize their future use in this setting. Finally, we must consider that by administering drugs known to interfere with inhibitors (like warfarin) or with the normal process of mineralization (like bisphosphonates), we can hypothetically favor or respectively prevent vascular calcifications.
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January 2012

Progression of coronary artery calcification in renal transplantation and the role of secondary hyperparathyroidism and inflammation.

Clin J Am Soc Nephrol 2009 Mar 11;4(3):685-90. Epub 2009 Feb 11.

Department of Clinical Science, University of Rome La Sapienza, Rome, Italy.

Background And Objectives: Transplantation should favorably affect coronary calcification (CAC) progression in dialysis; however, changes in CAC score in the individual patient are not reliably evaluated.

Design, Setting, Participants & Measurements: The authors used special tables of reproducibility limits for each score level to study, by multislice computed tomography and biochemistries, the 2-year changes in CAC in 41 transplant patients (age 48 +/- 13 yr, 25 men, dialysis vintage 4.8 +/- 4.3 yr, underwent transplant 6.2 +/- 5.5 yr prior). Thirty balanced dialysis patients served as controls.

Results: In the study group, Agatston score was stable, and C-reactive protein decreased, whereas fetuin and osteoprotegerin increased. In the control group, Agatston score increased, parathyroid hormone and phosphate decreased, and inflammation markers were persistently twice as high as in the study group. With regard to individual changes, 12.2% transplant patients worsened, compared with 56.6% of patients in dialysis (P < 0.0001). Patients without calcification at entry showed slower progression in transplantation (8.3%) than in dialysis (44.4%; P < 0.034), and the difference was similar to that observed in cases with CAC (17.6% versus 61.9%; P < 0.007). Discriminant analysis indicated parathyroid hormone, the modality of therapy (dialysis or transplantation), and erythrocyte sedimentation rate as the variables most associated with worsening.

Conclusions: Renal transplantation lowers but does not halt CAC progression. Inflammation and hyperparathyroidism are associated with progression in the populations studied.
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http://dx.doi.org/10.2215/CJN.03930808DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2653657PMC
March 2009